Andrew Brown

Under conditions of physiological stress, officers are sometimes required to make split-second life-or-death decisions, where deficits in performance can have tragic outcomes, including serious injury or death and strained police–community relations. The current study assessed the performance of 122 active-duty police officers during a realistic lethal force scenario to examine whether performance was affected by the officer’s level of operational skills training, years of police service, and stress reactivity. Results demonstrated that the scenario produced elevated heart rates, as well as perceptual and cognitive distortions, such as tunnel vision, commensurate with those observed in naturalistic use of force encounters. The average performance rating from the scenario was 59%, with 27% of participants making at least one lethal force error. Elevated stress reactivity was a predictor of poorer performance and increased lethal force errors. Level of training and years of police service had differential and complex effects on both performance and lethal force errors. Our results illustrate the need to critically reflect on police training practices and continue to make evidence-based improvements to training. The findings also highlight that while training may significantly improve outcomes, flawless performance is likely not probable, given the limits of human performance under stress. Implications for the objective reasonableness standard, which is used to assess the appropriateness of force in courts of law, are discussed.

Sterols and the reductant nicotinamide adenine dinucleotide phosphate (NADPH), essential for eukaryotic life, arose because of, and as an adaptation to, rising levels of molecular oxygen (O2). Hence, the NADPH and O2‐intensive process of sterol biosynthesis is inextricably linked to redox status. In mammals, cholesterol biosynthesis is exquisitely regulated post‐translationally by multiple E3 ubiquitin ligases, with membrane associated Really Interesting New Gene (RING) C3HC4 finger 6 (MARCHF6) degrading at least six enzymes in the pathway. Intriguingly, all these MARCHF6‐dependent enzymes require NADPH. Moreover, MARCHF6 is activated by NADPH, although what this means for control of cholesterol synthesis is unclear. Indeed, this presents a paradox for how NADPH regulates this vital pathway, since NADPH is a cofactor in cholesterol biosynthesis and yet, low levels of NADPH should spare cholesterol biosynthesis enzymes targeted by MARCHF6 by reducing its activity. We speculate MARCHF6 helps mammalian cells adapt to oxidative stress (signified by low NADPH levels) by reducing degradation of cholesterogenic enzymes, thereby maintaining synthesis of protective cholesterol.